Diabetic And Insulin
Diabetes mellitus
is a chronic disease characterized by relative or absolute
deficiency of insulin, resulting in glucose intolerance. It
occurs in 4-5 million persons in the United States
(approximately 2% of the population). The classic symptoms
of diabetes mellitus result from abnormal glucose
metabolism. The lack of insulin activity results in failure
of transfer of glucose from the plasma into the cells. This
situation so called “starvation in the midst of plenty”. The
body responds as if it were in the fasting state, with
stimulation of glucogenolysis, gluconeogenesis and lipolysis
producing ketone bodies.
The glucose
absorbed during a meal is not metabolized at the normal rate
and therefore accumulates in the blood (hyperglycemia) to be
excreted in the urine (glycosuria). Glucose in the urine
causes osmotic diuresis, leading to increase urine
production (polyuria). Stimulation of protein breakdown to
provide amino acids for gluconeogenesis results in muscle
wasting and weight loss. These classic symptoms occur only
in patients with severe insulin deficiency, most commonly in
type I diabetes. Many patients with type II diabetes do not
have these symptoms and present with one of the
complications of diabetes.
Generally, there
are two types of diabetes: Type I Diabetes Mellitus
(insulin- dependent diabetes mellitus, IDDM) and Type II
Diabetes Mellitus (non-insulin- dependent diabetes mellitus,
NIDDM).
Type I Diabetes
Mellitus (insulin- dependent diabetes mellitus, IDDM) is due
to destruction of pancreatic B cells. The cause of B cell
destruction in type I diabetes is unknown. A few cases have
followed viral infections, most commonly with coxsakievirus
B or mumps virus. Autoimmunity is believed to be the major
mechanism involved. Islet cell autoantibodies are present in
the serum of 90% of newly diagnosed cases. Such antibodies
are directed against several cell components, including
cytoplasmic and membrane antigens or against insulin itself
(IgG and IgE antibodies). Sensitized T lymphocytes with
activity against B cells have also been demonstrated in some
patients.
Plasma insulin
levels are very low or even absent in type I diabetes, and
ketoacidosis develops if the patients do not receive
exogenous insulin. Type I diabetes occurs most commonly in
juveniles, with the highest incidence worldwide among the
10- to 14-year-old group, but occasionally occurs in adults,
especially the nonobese and those who are elderly when
hyperglycemia first appears.
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